This dissertation contains three general components, each investigating an aspect of internal shear load redistribution within tendon, especially around defects. The first section investigates the mechanical response of tendon to partial lacerations of various depths, the second portion explores multiple aspects of the shear transfer internal loading mechanism of tendon, and the final section provides information regarding the cellular response to shear loading within tendon.

In the first section, cyclic and stress relaxation tests were performed on tendons before and after the introduction of a transverse, mid-substance partial laceration to a specified depth. Average stress within the remaining intact portion of the tendon initially decreased after laceration but exhibited a large increase in stress concentration when the laceration depth reached approximately 50% of the tendon width. Nominal stress and stiffness (calculated using the intact cross-sectional area) continually decreased with increasing laceration depth, although the decrease was not proportional to the percent loss of cross-sectional area. This result suggests the presence of a loading mechanism, i.e. shear, within tendon in addition to axial loading of individual components of the tendon hierarchy.

In the second portion of this dissertation, various aspects of shear load transfer within tendon were investigated by testing intact tendons and fascicles, those subject to overlapping lacerations on opposite ends of the specimens (introducing internal shear transfer), and contacting fascicle pairs gripped and pulled from opposite ends (requiring shear transfer to occur between fascicles). Comparing functionally distinct tendons, porcine flexor tendons (generally functioning at high stresses in vivo) and rat tail tendons (generally functioning under low stresses and used primarily as positional tendons in vivo) were both shown to maintain about 20% of the intact tendon stress when subject to overlapping lacerations (no intact fascicles end to end). However, the low stress, rat tail tendons had a more rapid decline in post-laceration maximum stress and modulus parameters with increasing laceration depth and a more linear, less tightly packed fascicular structure. Comparing shear transfer between tendon hierarchical levels, greater failure load and stiffness were seen between fibers than between fascicles. Approximately 33% of the longitudinal strength of the intact fascicle was maintained when overlapping lacerations were introduced to the fascicle. Within the fascicle, visualization of the shear transfer deformation mechanisms, completed by placing fiducial marks on specimens prior to stretch, uncovered the presence of both shear-lag and slip (sliding) between fibers, with slip present as the largest component of longitudinal deformation. Conversely, slip was seen between tendon fascicles at the inter-fascicular interface, with negligible shear-lag present.

The third, and final, component of this dissertation investigated the cellular viability of tenocytes within mechanically tested and not tested intact and lacerated fascicles. Mechanical testing consisted of cyclic loading to 4% strain for 10 cycles. Fascicles were subject to one of the following:​ a partial, mid-substance, transverse laceration (single laceration), longitudinally separated overlapping lacerations (double laceration), or remained intact for testing. Mechanically, peak load, steady state load, and stiffness decreased from the intact to single laceration to double laceration groups. Approximately 45% of the intact values were maintained when fascicles were subject to double lacerations (eliminating all fibers stretching the whole length of the fascicle). Cellularly, a large decrease in viability was seen in both single and double laceration groups, with the cell death primarily occurring within a longitudinal plane. This plane corresponded to high shear load transfer and extended far from the laceration site.